| Project/Area Number |
18K09661
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 57050:Prosthodontics-related
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
後藤 崇晴 徳島大学, 大学院医歯薬学研究部(歯学域), 助教 (00581381)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 歯科用金属アレルギー / 上皮角化細胞 / 細胞遊走 / 金属アレルギー / 樹状細胞 / ケモカイン / 口腔粘膜疾患 |
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| Outline of Final Research Achievements |
The purpose of this study was to clarify the mechanism of skin and mucosal lesion formation in dental metal allergy by analyzing the network between dendritic cells, T cells, and keratinocytes stimulated with metal antigens. The expression of semaphorin 7A was significantly enhanced on keratinocytes stimulated with nickel. The expression of semaphorin 7A was also enhanced in the ear skin of model mice, and the allergic reaction was attenuated when the expression of semaphorin 7A was inhibited. In addition, the expression of CCL20 and CXCL1, which promote inflammatory cell infiltration, was enhanced in allergic ear skin.
These results suggest that semaphorin 7A is essential for the allergic reaction to nickel, especially in the effector phase.
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| Academic Significance and Societal Importance of the Research Achievements |
金属アレルギーは比較的長年にわたり患者を苦しめる免疫疾患であり，近年では認知度も高まっている．それにもかかわらず，これまでの研究は症例報告を主体とした疫学研究に偏っており，病態の本質的な解明を試みたものはほとんどない．
本研究では，ニッケルアレルギーモデルマウスを用いて，アレルギー発症機序の端緒となる上皮への金属付着から続いて起こるセマフォリン7Aを主体とした細胞間のネットワークの一部を明らかにした．アレルギー発症の初めの部分を解明し制御することが可能であれば，このネットワークの制御を活かした治療方法の開発に寄与できるものと考える．
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